Evaluation of serum miR-221/222 as novel tumor markers
Ontology highlight
ABSTRACT:
DISEASE(S): Esophageal Cancer, Gastric Cancer, Colorectal Cancer, Pancreatic Cancer, Bile Duct Cancer, And Healthy Controls
PROVIDER: 2630284 | ecrin-mdr-crc |
REPOSITORIES: ECRIN MDR
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Project description:We studied 20 candidate genes (HCC hub genes, potential drug target genes, predominant somatic mutant genes) retrieved from available literature and public databases with potential to be used as biomarkers for the prognosis of HCC and prediction of treatment outcome. We analysed expression of the genes by RT-qPCR in 30 HCC tumor and adjacent non-tumor paired samples from Vietnamese patients.
2021-12-25 | GSE191298 | GEO
Project description:BACKGROUND: Several in vitro assays have been used to identify “cancer stem cells” (CSC), including expression of cell surface markers and Hoechst dye efflux properties. However, each of these methods has potential pitfalls that complicate interpretation of the results. Focusing on colon cancers (CC), the CD133 antigen has been proposed as a marker of colon CSC. However, conflicting results have been reported in the literature indicating the need of a systematic analysis of CSC within CC and a complete validation of markers for the isolation of these cells. AIMS: Aim of this study was to confirm that CD133 expression is a valid method for isolating CSC in CC and verify if other antigens can increase the specificity of this marker for isolating CSC in CC. METHODS: CD133+ and CD133- cells were isolated from different human CC lines (CaCo-2, HT29, LOVO, HCT-116) by FACS sorter and the tumor-initiating potential of CD133+ cells was assessed in vitro, by soft-agar colony formation assay, and in vivo, upon transplantation into nude mice. Furthermore, the gene expression profile of CD133+ versus CD133- CaCo-2 cells was compared by the means of microarray analysis. Then, in the effort to identify a common “tumor stem cell” signature for CC, the most relevant transcripts resulting from gene expression profiling on CD133+ cells was assessed by real-time PCR on SP-fraction isolated by FACS sorter from the same CC cell lines. Finally, we deplete CD133 expression in the CaCo-2 cell line by the means of siRNA and verified by Western Blot analysis whether there was a functional correlation between CD133 and the target genes. Moreover, CaCo-2 and HCT116 cells were exposed to sodium butyrate (NaBu) for 72h. Colon cells differentiation was assessed by Alkaline phosphatase activity and expression of CD133 and target genes was tested by western blot. RESULTS: We confirmed that only CD133+ cells have a tumor-initiating potential in vitro and in vivo. Furthermore, microarray analysis of CD133+ versus CD133- CaCo-2 cells revealed a significant overexpression of various transcripts involved in cell proliferation, invasion and stemness in CD133+ cell fraction. Comparison of the transcripts by real-time PCR revealed that the genes of Endothelin-1 (END-1) and NR4A2 are highly expressed in both CD133 + cells and in SP fractions. Finally, when we deplete CD133 expression in Caco-2cells by siRNA, we observed a significant attenuation of END-1 and NR4A2 expression, thus demonstrating that CD133 is involved in the transcriptional regulation of these genes. Interestingly, we also showed that the expression of all three genes was inversely correlated with cell differentiation status as demonstrated by the fact that their expression decreases in a time- and dose-dependent manner after differentiation induced by NaBu. CONCLUSION: Overall, this study confirms the role of CD133antigen as CSC marker and showed for the first time the existence of a functional relationship between CD133, END-1 and NR4A2 expression, hypothesizing that CD133 is involved in the transcriptional regulation of these gene. Microarray analysis was performed on CD133+ and CD133- sorted CACO-2 cells. For both fractions, cells were sorted three independent times. Sample preparation was performed according to Affymetrix recommendations. A total of 6 arrays were hybridized, including 3 CD133+ replicates and 3 CD133- replicates.
2011-01-04 | E-GEOD-24747 | biostudies-arrayexpress
Project description:ObjectiveHistological type is important for determining the management of patients with suspicious lung cancers. In this study, PET/CT combined with serum tumor markers were used to evaluate the histological type of lung lesions.Materials and methodsPatients with suspicious lung cancers underwent 18F-FDG PET/CT and serum tumor markers detection. SUVmax of the tumor and serum levels of tumor markers were acquired. Differences in SUVmax and serum levels of tumor markers among different histological types of lung cancers and between EGFR mutation statues of adenocarcinoma were compared. The diagnostic efficiencies of SUVmax alone, each serum tumor marker alone, combined tumor markers and the combination of both methods were further assessed and compared.ResultsSCC had the highest level of SUVmax, followed by SCLC and adenocarcinoma, and benign lesions had a lowest level. CYFRA21-1 and SCC-Ag were significantly higher in SCC, NSE was significantly higher in SCLC (P<0.001), and CEA was higher in adenocarcinoma (P = 0.343). The diagnostic efficiencies in evaluating histological types of suspicious lung cancers were insufficient when using each serum tumor marker or SUVmax alone. When combined, the AUC, sensitivity and specificity increased significantly (P<0.05 for all). Additionally, to adenocarcinoma, no significant difference was found between EGFR mutation statuses in SUVmax or serum tumor markers (P>0.05 for all).ConclusionsSUVmax and serum tumor markers show values in evaluating the histological types of suspicious lung cancers. When properly combined, the diagnostic efficiency can increase significantly.
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Project description:Objectives M-bM-^@M-^STo determine whether inflammation biomarkers can be used as indicators of therapeutic response, an exploratory study was performed to ascertain whether short term improvements in risk parameters will have measureable effects on a pre-defined panel of plaque inflammation biomarkers. Methods and Results M-bM-^@M-^S Patients (n=121) with peripheral arterial disease were enrolled into one of three sub-studies based upon the presence of hypercholesterolemia, hypertension, or diabetes. Patients were randomized to 6 weeks of drug treatment vs. placebo and underwent catheter excision of atherosclerotic tissue from one extremity at baseline and the contralateral extremity after treatment. Simvastatin 40mg once daily reduced LDL-C by 43% (p<0.01), losartan 50mg once daily reduced diastolic blood pressure by 4 mm Hg (p=0.099), and pioglitazone 30mg once daily reduced serum glucose by 66mg/dL (p=0.008). Despite these effects, there were no consistent treatment effects on a large panel of plaque protein, RNA and lipid biomarkers. Conclusions M-bM-^@M-^S Short term treatment with drugs that improve cardiovascular risk parameters did not result in a measureable reduction in the levels of peripheral arterial plaque inflammation biomarkers. Further studies are required to identify biomarkers that are sufficiently predictive to be used to identify drug candidates for testing in large cardiovascular outcome studies. (ClinicalTrials.gov: NCT00720577) Human peripheral atherosclerosis plaque was extracted from lower extremities, and RNA, lipids and proteins extracted. RNA was analyzed in an Agilent two-color platform.
2012-05-15 | E-GEOD-37824 | biostudies-arrayexpress
Project description:Sequencing technologies together with new bioinformatics tools have led to the complete sequencing of various genomes. However, information regarding the human transcriptome and its annotation is yet to be completed. The Human Cancer Genome Project, using ORESTES (open reading frame EST sequences) methodology, contributed to this major objective by generating data from about 1.2 million expressed sequence tags (ESTs). Approximately 30% of these sequences did not align to ESTs in the public databases and were considered no-match ORESTES. On the basis that a set of these ESTs could represent new transcripts, we constructed a cDNA microarray. This platform was used to hybridize against 12 different normal or tumor tissues. We identified 3,421 transcribed regions not associated with annotated transcripts, representing 83.3% of the platform. The total number of differentially expressed sequences, with fold differences between tumor and normal samples of at least two, in one or more different tissues, was 1,007. Also, about 28% of analyzed sequences could represent non-coding RNAs (ncRNAs). Our data reinforces the knowledge of the human genome being pervasively transcribed, and point out molecular marker candidates for different cancers. To reinforce our data, we confirmed, by real-time PCR, the differential expression of 3 out of 8 potentially tumor markers in prostate tissues. A list of 1,007 differentially expressed sequences, as well as the 291 potentially non-coding molecular markers for different tumors was provided. Experiments were performed in duplicate, using dye-swap method. We used linearly amplified RNA samples (T7-based protocol), derived from 56 normal or tumor tissues from 12 distincts body localization, and a pool of RNAs obtained from 15 distinct human cell lines as reference. cDNA was synthesized in the presence of aminoallyl-dUTP (Sigma-Aldrich) and labeled using Alexa Fluor 555 or Alexa Fluor 647 dyes (Invitrogen).
2009-04-13 | E-GEOD-12737 | biostudies-arrayexpress
Project description:Objectives –To determine whether inflammation biomarkers can be used as indicators of therapeutic response, an exploratory study was performed to ascertain whether short term improvements in risk parameters will have measureable effects on a pre-defined panel of plaque inflammation biomarkers. Methods and Results – Patients (n=121) with peripheral arterial disease were enrolled into one of three sub-studies based upon the presence of hypercholesterolemia, hypertension, or diabetes. Patients were randomized to 6 weeks of drug treatment vs. placebo and underwent catheter excision of atherosclerotic tissue from one extremity at baseline and the contralateral extremity after treatment. Simvastatin 40mg once daily reduced LDL-C by 43% (p<0.01), losartan 50mg once daily reduced diastolic blood pressure by 4 mm Hg (p=0.099), and pioglitazone 30mg once daily reduced serum glucose by 66mg/dL (p=0.008). Despite these effects, there were no consistent treatment effects on a large panel of plaque protein, RNA and lipid biomarkers. Conclusions – Short term treatment with drugs that improve cardiovascular risk parameters did not result in a measureable reduction in the levels of peripheral arterial plaque inflammation biomarkers. Further studies are required to identify biomarkers that are sufficiently predictive to be used to identify drug candidates for testing in large cardiovascular outcome studies. (ClinicalTrials.gov: NCT00720577)
2012-05-16 | GSE37824 | GEO
Project description:BACKGROUND: Several in vitro assays have been used to identify “cancer stem cells” (CSC), including expression of cell surface markers and Hoechst dye efflux properties. However, each of these methods has potential pitfalls that complicate interpretation of the results. Focusing on colon cancers (CC), the CD133 antigen has been proposed as a marker of colon CSC. However, conflicting results have been reported in the literature indicating the need of a systematic analysis of CSC within CC and a complete validation of markers for the isolation of these cells. AIMS: Aim of this study was to confirm that CD133 expression is a valid method for isolating CSC in CC and verify if other antigens can increase the specificity of this marker for isolating CSC in CC. METHODS: CD133+ and CD133- cells were isolated from different human CC lines (CaCo-2, HT29, LOVO, HCT-116) by FACS sorter and the tumor-initiating potential of CD133+ cells was assessed in vitro, by soft-agar colony formation assay, and in vivo, upon transplantation into nude mice. Furthermore, the gene expression profile of CD133+ versus CD133- CaCo-2 cells was compared by the means of microarray analysis. Then, in the effort to identify a common “tumor stem cell” signature for CC, the most relevant transcripts resulting from gene expression profiling on CD133+ cells was assessed by real-time PCR on SP-fraction isolated by FACS sorter from the same CC cell lines. Finally, we deplete CD133 expression in the CaCo-2 cell line by the means of siRNA and verified by Western Blot analysis whether there was a functional correlation between CD133 and the target genes. Moreover, CaCo-2 and HCT116 cells were exposed to sodium butyrate (NaBu) for 72h. Colon cells differentiation was assessed by Alkaline phosphatase activity and expression of CD133 and target genes was tested by western blot. RESULTS: We confirmed that only CD133+ cells have a tumor-initiating potential in vitro and in vivo. Furthermore, microarray analysis of CD133+ versus CD133- CaCo-2 cells revealed a significant overexpression of various transcripts involved in cell proliferation, invasion and stemness in CD133+ cell fraction. Comparison of the transcripts by real-time PCR revealed that the genes of Endothelin-1 (END-1) and NR4A2 are highly expressed in both CD133 + cells and in SP fractions. Finally, when we deplete CD133 expression in Caco-2cells by siRNA, we observed a significant attenuation of END-1 and NR4A2 expression, thus demonstrating that CD133 is involved in the transcriptional regulation of these genes. Interestingly, we also showed that the expression of all three genes was inversely correlated with cell differentiation status as demonstrated by the fact that their expression decreases in a time- and dose-dependent manner after differentiation induced by NaBu. CONCLUSION: Overall, this study confirms the role of CD133antigen as CSC marker and showed for the first time the existence of a functional relationship between CD133, END-1 and NR4A2 expression, hypothesizing that CD133 is involved in the transcriptional regulation of these gene.
2011-01-04 | GSE24747 | GEO
Project description:ImportanceSerum tumor markers carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA19-9), and cancer antigen 125 (CA125) have been useful in the management of gastrointestinal and gynecological cancers; however, there is limited information regarding their utility in patients with appendiceal adenocarcinoma.ObjectiveTo assess the association of serum tumor markers (CEA, CA19-9, and CA125) with clinical outcomes and pathologic and molecular features in patients with appendiceal adenocarcinoma.Design, setting, and participantsThis is a retrospective cohort study at a single tertiary care comprehensive cancer center. The median (IQR) follow-up time was 52 (21-101) months. Software was used to query the MD Anderson internal patient database to identify patients with a diagnosis of appendiceal adenocarcinoma and at least 1 tumor marker measured at MD Anderson between March 2016 and May 2023. Data were analyzed from January to December 2023.Main outcomes and measuresAssociation of serum tumor markers with survival in patients with appendiceal adenocarcinoma. Cox proportional hazards regression analyses were also performed to assess associations between clinical factors (serum tumor marker levels, demographics, and patient and disease characteristics) and patient outcomes (overall survival).ResultsA total of 1338 patients with appendiceal adenocarcinoma were included, with a median (range) age at diagnosis of 56.5 (22.3-89.6) years. The majority of the patients had metastatic disease (1080 patients [80.7%]). CEA was elevated in 742 of the patients tested (56%), while CA19-9 and CA125 were elevated in 381 patients (34%) and 312 patients (27%), respectively. Individually, elevation of CEA, CA19-9, or CA125 were associated with worse 5-year survival; elevated vs normal was 81% vs 95% for CEA (hazard ratio [HR], 4.0; 95% CI, 2.9-5.6), 84% vs 92% for CA19-9 (HR, 2.2; 95% CI, 1.4-3.4), and 69% vs 93% for CA125 (HR, 4.6; 95% CI, 2.7-7.8) (P < .001 for all). Quantitative evaluation of tumor markers was associated with outcomes. Patients with highly elevated (top 10th percentile) CEA, CA19-9, or CA125 had markedly worse survival, with 5-year survival rates of 59% for CEA (HR, 9.8; 95% CI, 5.3-18.0), 64% for CA19-9 (HR, 6.0; 95% CI, 3.0-11.7), and 57% for CA125 (HR, 7.6; 95% CI, 3.5-16.5) (P < .001 for all). Although metastatic tumors had higher levels of all tumor markers, when restricting survival analysis to 1080 patients with metastatic disease, elevated CEA, CA19-9, or CA125 were all still associated worse survival (HR for CEA, 3.4; 95% CI, 2.5-4.8; P < .001; HR for CA19-9, 1.8; 95% CI, 1.2-2.7; P = .002; and HR for CA125, 3.9; 95% CI, 2.4-6.4; P < .001). Interestingly, tumor grade was not associated with CEA or CA19-9 level, while CA-125 was slightly higher in high-grade tumors relative to low-grade tumors (mean value, 18.3 vs 15.0; difference, 3.3; 95% CI, 0.9-3.7; P < .001). Multivariable analysis identified an incremental increase in the risk of death with an increase in the number of elevated tumor markers, with an 11-fold increased risk of death in patients with all 3 tumor markers elevated relative to those with none elevated. Somatic mutations in KRAS and GNAS were associated with significantly higher levels of CEA and CA19-9.Conclusions and relevanceIn this retrospective study of serum tumor markers in patients with appendiceal adenocarcinoma, CEA, CA19-9, and CA125 were associated with overall survival in appendiceal adenocarcinoma. Given their value, all 3 biomarkers should be included in the initial workup of patients with a diagnosis of appendiceal adenocarcinoma.
| S-EPMC10902735 | biostudies-literature
Project description:Microarray expression arrays on mesothelium and other tissues dissected from mice were used to identify candidate mesothelial lineage markers. These were then tested by qRTPCR across a panel of human mesothelioma cells lines, other cancers, and normal primary cells includidng mesothelial cells. Twenty four samples were analysed, composed of 8 tissues in triplicate
2011-12-18 | E-GEOD-30793 | biostudies-arrayexpress
Project description:Interventions: Group 1: Observational Study with diagnostic intervention: the participants will be asked to donate a blood sample, 2 native stool samples and to perform 2 FIT and one Hemoccult test.
Primary outcome(s): sensitivity and specificity of tests for the detection of advanced colorectal neoplasia
Study Design: Allocation: N/A: single arm study; Masking: Open (masking not used); Control: uncontrolled; Assignment: single; Study design purpose: diagnostic
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